Diabetes mellitus (DM) is a chronic metabolic disease associated with numerous vascular complications including impaired wound healing. Microvascular complications associated with T2D may lead to, for example, limb amputation and increased risk of mortality. Chronic non-healing ulcers in diabetic patients localized on pressure points of the foot is a major cause of non-traumatic lower leg amputation.1 These ulcers occur not only in the later stages of diabetes but are also seen in newly diagnosed patients. Accumulating studies focus on promoting angiogenesis, or the formation of blood vessels from pre-existing ones, to promote wound healing in diabetic mouse models.2-5 Progression of angiogenesis is controlled by a balance between pro- and anti-angiogenic factors. Wound healing requires vascular ECs need to be rapidly activated to migrate to distant sites and proliferate in order to form new primary capillaries from existing ones in response to an angiogenic stimuli.6 Failure to do so may delay tissue repair in an array of pathological or physiological conditions. Growth factors such as vascular endothelial cell growth factor (VEGF), tumor necrosis factor-α (TNF-α), basic fibroblast growth factor (bFGF), or placenta growth factor (PIGF) are potent regulators of angiogenesis. Impaired EC angiogenic responses have been linked to exacerbation of a wide range of disease states including diabetic wound healing.7 